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- Publisher Website: 10.1093/europace/eux312
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Article: Genetically deprived vitamin D exposure predisposes to atrial fibrillation
Title | Genetically deprived vitamin D exposure predisposes to atrial fibrillation |
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Authors | |
Keywords | 25-Hydroxyvitamin D Atrial fibrillation Genetic polymorphism Vitamin D-binding protein |
Issue Date | 2017 |
Citation | EP Europace, 2017, v. 19, p. iv25-iv31 How to Cite? |
Abstract | Aims:
Low vitamin D level is associated with atrial fibrillation (AF) and may be implicated in its pathogenesis.
Methods and results:
We studied single nucleotide polymorphisms (SNPs) of vitamin D mechanistic pathways and serum 25-hydroxyvitamin D [25(OH)D] levels in an age- and gender-matched case–control study (controls without AF: mean age 68.6 ± 8.7 years, female 25%; n = 1019; with AF: mean age 69.7 ± 9.5 years, female 30%; n = 156) recruited from a Chinese clinical cohort of patients with stable coronary artery disease. Twelve SNPs involved in the vitamin D mechanistic pathways were studied [biosynthetic: rs4646536, rs10877012, rs3829251, rs1790349; activation: rs2060793, rs1993116; vitamin D-binding protein (VBP)/group-specific component (GC): rs4588, rs7041, rs2282679, rs1155563; and vitamin D receptor: rs1544410, rs10735810]. A genetic risk score (GRS) (0–8) was constructed from SNPs associated with serum 25(OH)D as a proxy to lifelong vitamin D-deficient state. All 4 SNPs involved in the VBP/GC were significantly associated with serum 25(OH)D (rs4588, P < 0.001; rs2282679, P < 0.001; rs7041, P = 0.011; rs1155563, P < 0.001; all other SNPs, P > 0.05). Vitamin D GRS (points 0–8) generated from these 4 SNPs was independently predictive of serum 25(OH)D [B = 0.54, 95% confidence interval (CI) 0.30–0.79; P < 0.001]. Genetically deprived vitamin D status as denoted by a low GRS (0–3) independently predicted an increased risk of AF, compared to a high GRS (4–8) (odds ratio = 1.848, 95% CI 1.217–2.805; P = 0.004).
Conclusion:
Genetically deprived vitamin D exposure predisposes to increased AF among patients with coronary artery disease. Whether VBP/GC may alter the risk of AF via alternative mechanisms warrants further studies. |
Persistent Identifier | http://hdl.handle.net/10722/250521 |
ISSN | 2023 Impact Factor: 7.9 2023 SCImago Journal Rankings: 2.895 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Chan, YH | - |
dc.contributor.author | Yiu, KH | - |
dc.contributor.author | Hai, SHJJ | - |
dc.contributor.author | Chan, PHM | - |
dc.contributor.author | Lam, TH | - |
dc.contributor.author | Cowling, BJ | - |
dc.contributor.author | Sham, PC | - |
dc.contributor.author | Lau, CP | - |
dc.contributor.author | Lam, KSL | - |
dc.contributor.author | Siu, DCW | - |
dc.contributor.author | Tse, HF | - |
dc.date.accessioned | 2018-01-18T04:28:21Z | - |
dc.date.available | 2018-01-18T04:28:21Z | - |
dc.date.issued | 2017 | - |
dc.identifier.citation | EP Europace, 2017, v. 19, p. iv25-iv31 | - |
dc.identifier.issn | 1099-5129 | - |
dc.identifier.uri | http://hdl.handle.net/10722/250521 | - |
dc.description.abstract | Aims: Low vitamin D level is associated with atrial fibrillation (AF) and may be implicated in its pathogenesis. Methods and results: We studied single nucleotide polymorphisms (SNPs) of vitamin D mechanistic pathways and serum 25-hydroxyvitamin D [25(OH)D] levels in an age- and gender-matched case–control study (controls without AF: mean age 68.6 ± 8.7 years, female 25%; n = 1019; with AF: mean age 69.7 ± 9.5 years, female 30%; n = 156) recruited from a Chinese clinical cohort of patients with stable coronary artery disease. Twelve SNPs involved in the vitamin D mechanistic pathways were studied [biosynthetic: rs4646536, rs10877012, rs3829251, rs1790349; activation: rs2060793, rs1993116; vitamin D-binding protein (VBP)/group-specific component (GC): rs4588, rs7041, rs2282679, rs1155563; and vitamin D receptor: rs1544410, rs10735810]. A genetic risk score (GRS) (0–8) was constructed from SNPs associated with serum 25(OH)D as a proxy to lifelong vitamin D-deficient state. All 4 SNPs involved in the VBP/GC were significantly associated with serum 25(OH)D (rs4588, P < 0.001; rs2282679, P < 0.001; rs7041, P = 0.011; rs1155563, P < 0.001; all other SNPs, P > 0.05). Vitamin D GRS (points 0–8) generated from these 4 SNPs was independently predictive of serum 25(OH)D [B = 0.54, 95% confidence interval (CI) 0.30–0.79; P < 0.001]. Genetically deprived vitamin D status as denoted by a low GRS (0–3) independently predicted an increased risk of AF, compared to a high GRS (4–8) (odds ratio = 1.848, 95% CI 1.217–2.805; P = 0.004). Conclusion: Genetically deprived vitamin D exposure predisposes to increased AF among patients with coronary artery disease. Whether VBP/GC may alter the risk of AF via alternative mechanisms warrants further studies. | - |
dc.language | eng | - |
dc.relation.ispartof | EP Europace | - |
dc.subject | 25-Hydroxyvitamin D | - |
dc.subject | Atrial fibrillation | - |
dc.subject | Genetic polymorphism | - |
dc.subject | Vitamin D-binding protein | - |
dc.title | Genetically deprived vitamin D exposure predisposes to atrial fibrillation | - |
dc.type | Article | - |
dc.identifier.email | Yiu, KH: khkyiu@hku.hk | - |
dc.identifier.email | Hai, SHJJ: haishjj@hku.hk | - |
dc.identifier.email | Chan, PHM: phmchan@hku.hk | - |
dc.identifier.email | Lam, TH: hrmrlth@hkucc.hku.hk | - |
dc.identifier.email | Cowling, BJ: bcowling@hku.hk | - |
dc.identifier.email | Sham, PC: pcsham@hku.hk | - |
dc.identifier.email | Lau, CP: cplau@hkucc.hku.hk | - |
dc.identifier.email | Lam, KSL: ksllam@hku.hk | - |
dc.identifier.email | Siu, DCW: cwdsiu@hkucc.hku.hk | - |
dc.identifier.email | Tse, HF: hftse@hkucc.hku.hk | - |
dc.identifier.authority | Yiu, KH=rp01490 | - |
dc.identifier.authority | Hai, SHJJ=rp02047 | - |
dc.identifier.authority | Chan, PHM=rp01864 | - |
dc.identifier.authority | Lam, TH=rp00326 | - |
dc.identifier.authority | Cowling, BJ=rp01326 | - |
dc.identifier.authority | Sham, PC=rp00459 | - |
dc.identifier.authority | Lam, KSL=rp00343 | - |
dc.identifier.authority | Siu, DCW=rp00534 | - |
dc.identifier.authority | Tse, HF=rp00428 | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1093/europace/eux312 | - |
dc.identifier.scopus | eid_2-s2.0-85040073298 | - |
dc.identifier.hkuros | 284003 | - |
dc.identifier.volume | 19 | - |
dc.identifier.spage | iv25 | - |
dc.identifier.epage | iv31 | - |
dc.identifier.eissn | 1532-2092 | - |
dc.identifier.isi | WOS:000417738300004 | - |
dc.identifier.issnl | 1099-5129 | - |